Researchers from the University of Colorado School of Medicine have identified a potential therapeutic target for treating obesity and diabetes. The scientists studied the biological function of an epigenetic modifier known as histone deacetylase 11 (HDAC11) and determined that deleting it in mice stimulates the formation of brown adipose tissue. The absence of HDAC11 also triggered beiging of white adipose tissue. These changes are important because white adipose tissue stores energy, while brown adipose tissue produces heat, thus expending energy.

The study, ‘HDAC11 suppresses the thermogenic program of adipose tissue via BRD2’, published in JCI Insight, reveal a regulatory node that could lead to the development of a pharmaceutical-based therapy for obesity and metabolic disease based on increasing energy expenditure.

"The findings uncovered a druggable transcriptional pathway for regulation of energy expenditure, and thus suggest novel approaches for combating the global pandemics of obesity and diabetes based on HDAC11 inhibition," said Dr Timothy A McKinsey, associate professor of medicine in the Division of Cardiology, who is the corresponding author of the article.

Mice lacking HDAC11 were protected from obesity, insulin resistance and other effects of high-fat feeding. The findings suggest a previously unrecognized role for HDAC11, and an associated protein known as BRD2, in the control of adipose tissue.

"Through our investigation we found that inhibiting HDAC11 increases energy expenditure, which highlights its potential as a target in obesity and metabolic disease therapeutic strategies," added McKinsey. "We now need to test the role of HDAC11 in large animal models of metabolic disease and in human cell systems as we attempt to translate these exciting findings to the clinic."